The precise cause of peptic ulceration in man is unknown although gastric acid is considered to be one of the essential factors in the etiology of this disease. It recently was discovered that gastric acid secretion is mediated, at least in part, by histamine H.sub.2 -receptors located on parietal cells in the gastric mucosa and that gastric acid output induced by all secretagogues could be antagonized by specific antagonists of these receptors [Black, J. W. et al., Nature, 236, 385-390 (1972); Brimblecombe, R. W. et al., J. Int. Med. Res., 3, 86-92 (1975)]. The first successful commercial histamine H.sub.2 -receptor antagonist, cimetidine, is now in widespread use as an antiulcer agent. Etintidine (BL-5641) is a new histamine H.sub.2 -receptor antagonist which is about twice as potent as cimetidine [Cavanagh, R. L. et al., Fed. Proc., 39, 768 (1980)].
The role of the proteolytic enzyme, pepsin, in the etiology of ulceration is not completely understood. Pepsin has been shown to play a major role in the development of experimentally induced ulcers in animals, but this may be due to lesion enlargement by means of pepsin digestion of necrotic tissue rather than by causing the initial damage. It is also possible that pepsin is entirely responsible for the erosions and that the acid produces pain and retards healing.